NOD mice spontaneously develop insulin-dependent diabetes mellitus (IDDM) secondary to immunologically-mediated beta cell destruction in pancreatic islets. Shortly after the appearance of diabetes, NOD mice developed renal lesions consisting of diffuse mesangial sclerosis, thickening of glomerular basement membranes, and albuminuria. These lesions closely mimic those of IDDM in humans. Morphometric analysis showed that the kidney weight and glomerular size were increased in diabetic mice, compared to non-diabetic mice, and that the ratio glomerular volume/kidney weight was elevated in diabetic mice. These findings suggest that this disproportionate increase in glomerular size may play an important role in the development of diabetic nephropathy.